Alzheimer’s disease is known for causing serious problems in the brain, such as memory loss, confusion, and difficulty thinking clearly.
One of the main things that happen in the brains of people with Alzheimer’s is the buildup of a sticky protein called tau. When tau becomes too active, it collects too many phosphate molecules in a process called hyperphosphorylation.
This causes tau to stick together and form twisted clumps, also called tangles, inside brain cells. These tangles block the brain cells from working properly and eventually cause them to die.
Now, new research from scientists at Mass General Brigham has found that these harmful tangles might actually be part of the brain’s natural way of protecting itself—especially from viruses. The study, published in the journal Nature Neuroscience, gives us a new and surprising way to think about how Alzheimer’s disease may begin.
Dr. Rudolph Tanzi, the senior author of the study, said that he had always wondered why humans developed gene mutations that seem to lead to Alzheimer’s disease. He explained that our ancestors, who lived much shorter lives than we do today, may have had a survival advantage from these genes.
Back when people rarely lived past the age of 30, the changes in the brain caused by things like amyloid plaques and tau tangles may have actually helped fight off dangerous infections.
Tanzi and his team believe that the proteins involved in Alzheimer’s disease, including both amyloid beta and tau, might have started out as part of a natural defense system in the brain. In earlier studies, they found that amyloid beta can kill bacteria and viruses. Now, they think tau might do something similar.
To explore this idea, the researchers studied human brain cells in the lab and exposed them to a common virus called HSV1, or herpes simplex virus type 1. This is the virus that causes cold sores but can also infect the brain.
They found that after the virus entered the brain cells, the tau protein became hyperphosphorylated and started to form tangles—just like what happens in Alzheimer’s disease.
But here’s the interesting part: the researchers also discovered that the tau protein was able to stick to the outer shell of the virus and stop it from spreading. When infected, the brain cells released this sticky form of tau, which trapped the virus and protected other cells from being attacked.
According to the lead author Dr. William Eimer, this means that tau might be acting like an antiviral protein, helping the brain defend itself. He suggests that the tangles we see in Alzheimer’s patients could have originally formed as a way to stop viruses from jumping from one brain cell to another.
In short, the findings of this study offer a whole new way to understand the brain changes that happen in Alzheimer’s disease. What we often see as damage might actually be part of the brain’s natural defense system—a system that worked well when people lived shorter lives, but now causes problems as people grow older.
This discovery could help scientists think of new ways to treat or even prevent Alzheimer’s by focusing on the brain’s immune response to infections.
If you care about Alzheimer’s, please read studies about Scientists find the root cause of Alzheimer’s disease and findings of Alzheimer’s might not be primarily a brain disease. A new theory suggests it’s an autoimmune condition.
If you care about Alzheimer’s disease, please read studies about These places in U.S. have the most cases of Alzheimer’s disease and findings of Scientists confirm the link between COVID-19 and Alzheimer’s disease.
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